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PMCOL 343 > 2-cardio > Flashcards

2-cardio Flashcards

1
Q

what is the role of the sinoatrial node

A

its the fastest pacemaker and dominates the rhythm normally

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2
Q

what is the fastest pacemaker of the heart

A

SA node(cells have the quickest rate of spontaneous depolarization, thus they initiate action potentials the quickest)

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3
Q

what is the role of the atrioventricular node node (3)

A

secondary pacemaker, takes over if SA node is damaged

protects ventricles from excessive electrical activity in supraventricular tissues

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4
Q

what part of the heart protects from excessive electrical activity in supraventricular tissues

A

the AV node

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5
Q

what is the role of the purkinje fibres

A

some pacemaker activity, can help if both SA AV node fail

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6
Q

what are the 3 phases of normal cardiac activity (simple)

A

atrial systole, delay, ventricular systole

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7
Q

where does the impulse originate that causes contraction of all the ventricles

A

SA node

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8
Q

what are the 6 steps of cardiac activity starting from SA node to ventricular contraction

A 
1-impulse from SA node
2-atrial contraction
3-AV node
4-bundle of His
5-Purkinje fibres
6-ventricles contract
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9
Q

what does “extinguish by collision” mean and why do you need it

A

impulses from SA node divide and pass through the heart, causes collisions with all the impulses so they stop

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10
Q

what happens if the SA node impulse is not extinguished

A

then there may be extra beats or dysrhythmias

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11
Q

what can cause dysrhytmias (general)

A

when the timing of impulse passing or conduction is disturbed

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12
Q

what is the definition of dysrythmia

A

changes in normal cardiac rhythm

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13
Q

what can cause dysrhythmias (4 causes)

A

delayed after depolarization
abnormal pacemaker activities
heart block
re-entry

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14
Q

what is heart block/what causes it

A

SA fails so purkinje and AV can make contractions but they are out of pace

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15
Q

what are symptoms of dysrhythmias

A

palpatations, fainting or asymptomatic

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16
Q

can dysrhythmias be fatal

A

yes

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17
Q

how do you name dysrhythmias

A

named after point of origin
ex: atrial dysrhythmias
ventricular dysrhythmias

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18
Q

what is the order of flutter tachycardia and fibrillation from most to least impulses per min

A

fibrillation>flutter>tachycardia

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19
Q

what do supra ventricular dysrhythmias do to the heart (where affected)

A

ventricular contraction is effected but the issue is from places above (supra) the ventricles

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20
Q

are ventricular dysrhythmias or supraventricular dysrhythmias more dangerous than supraventricular

A

ventricular dysrhythmias

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21
Q

when do you use AV blocking drugs

A

for superventricular dysrhythmias

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22
Q

can you use AV blockers for superventricular dysrhythmias

A

yes its ideal

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23
Q

can you use AV blockers for ventricular dysrhythmias

A

no

you want to get it back to normal sinus rhythm

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24
Q

where are the “fast” cardiac action potentials

A

purkinje fibres, atria, ventricles

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25
Q

where are the “slow” cardiac action potentials

A

SA and AV nodes

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26
Q

what happens in phase 0 of purkinje AP

A

Na goes in (rapid depolarization)

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27
Q

what happens in phase 1 of purkinje AP

A

Na goes in to a lesser extent, L type ca channels open

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28
Q

what happens in phase 2 of purkinje AP

A

-Na Ca go through ion channels
-electrogenic na/ca exchange operates (3na in 1 ca out)
“plateau”

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29
Q

what happens in phase 3 of purkinje AP

A

K goes out (final repolarization)

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30
Q

what happens in phase 4 of purkinje AP

A

pacemaker depolarization

  • Na K dependent
  • activation of HCN channels
  • NaK pump restores ionic gradient
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31
Q

what happens in phase 0 of SA node AP

A

Ca++ and Na+ go in

32
Q

what happens in phase 1 of SA node AP

A

doesnt exist

33
Q

what happens in phase 3 of SA node AP

A

K+ goes out

34
Q

what happens in phase 2 of SA node AP

A

doesnt exist

35
Q

what happens in phase 4 of SA node AP

A

Ca++ dependent pacemaker

36
Q

does purkinje or SA node have a more Ca++ dependent action potential

A

SA node more Ca++

37
Q

what is APD

A

action potential duration

38
Q

what is ERP

A

effective refractory period

39
Q

can tissue respond to stimulus during refractory perioud

A

no

40
Q

what is the relationship between ADP and ERP

A

if ADP increases then ERP increases too

other way around too

41
Q

what is the P wave

A

atrial depolarization

42
Q

what is the QRS complex

A

ventricular depolarization

43
Q

what is the T wave

A

ventricular repolarization

44
Q

what is the PR interval

A

AV conduction time

45
Q

what is the QT interval

A

duration of ventricular AP

46
Q

what are 2 directions that impulses can travel

A

in normal or retrograde direction (so like forwards and backwards)

47
Q

what happens to impulse direction with damaged tissue

A

normal conduction blocked BUT retrograde impulses propagate slowly

48
Q

what is worse - no conduction in heart or a blocked normal conduction and slow retrograde

A

when its block normal and slow retrograde

49
Q

what happens with a one way conduction block (what does it cause)

A

dysrhythmia

50
Q

which adrenergic receptors are found in the heart

A

beta1

51
Q

where are b1 receptors in the heart

A

all parts!

52
Q

how are b1 effects of the heart mediated

A 
by Gs
 (adenylyl cyclase, cAMP, phosphorylation of ion channels via PKA)
53
Q

what causes the positive chronotropic effect (general)

A

the effect of b1 adrenergics on the heart

54
Q

what happens specifically in the positive chronotropic effect (2)

A

increase of slope of phase 4 pacemaker in SA node

resting membrane potential gets to threshold sooner

55
Q

what causes the positive ionotropic effect

A

increase ca influx through L type ca channels in phase 2 = more contraction (more calcium=more contraction)

56
Q

what happens to AV conduction with b1 agonist and what does it cause

A

decreases PR interval (increase AV conduction)

enables high HR but can lead to dysrhythmia

57
Q

what do b1 agonists do to ventricular AP duration

A

enables high HR but can lead to dysrhythmia (can make AP shorter to get more impulses in but overstimulation can cause dysrhythmia)

58
Q

what do b1 agonists do to purkinje fibre (2)

A

increase its rhythmicity (increases slope so it gets to threshold sooner)

good for emergency pacemaker but can lead to dysrhythmias

59
Q

when do early afterdepolarizations occur

A

in the platea

60
Q

when do late afterdepolarizations occur

A

from resting potential

61
Q

what causes late and early afterdepolarizations to occur

A

calcium overload, so then excess activation of Na/Ca exchanger!!1

62
Q

what can happen with late and early afterdepolarizations

A

dysrhythmias

63
Q

what is transporter in the Na Ca exchanger and where

A

3na in

1ca out

64
Q

what nerve is the main parasympathetic nerves in the heart

A

vagus nerve

65
Q

where does the vagus nerve go in the heart

A

only goes to supraventricular tissue

66
Q

where do sympathetic nerves go to the heart

A

everywhere

67
Q

what types of receptors mediate parasympathetic effects on heart

A

M2 receptors (muscarinic)

68
Q

what g protein is M2

A

Gi

69
Q

what causes the negative chronotropic effect (general)

A

M2 agonists onto the heart

70
Q

what 3 main things happen in the negative chrontropic effect

A

SA node slows
M2 hyperpolarizes SA node (activates GIRK)
decrease slope of pahse 4 pacemaker

71
Q

what are 6 main effects of b1 agonists on heart

A
  • positive chonotropic effect
  • positive inotropic effect
  • AV conduction increase
  • shorten ventricular AP duration
  • increase purkinje fiber rhythmicity
  • facilitation of generations of early/late afterdepolarization
72
Q

what are 3 main effects of M2 on heart

A
  • negative chronotropic effect
  • atria shortens AP & refractory
  • AV node increases PR interval
73
Q

what does M2 do to atria

A

shortens AP duration and reduces refractory period

74
Q

what does M2 do to AV node

A

conduction block or delay, increased PR interval

75
Q

why does AV conduction increase with beta adrenergics

A

because they increase SA node so the ventricles gotta keep up

76
Q

what does atropine do to heart

A

tachycardia and increased AV conduction

PMCOL 343 (31 decks)

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